Reduction of acoustically-induced auditory impairment by inhalation of carbogen gas. I. Permanent noise-induced cochlear damage.
The possible beneficial effects of carbogen gas (95% O2/5% CO2) inhalation on noise-induced permanent cochlear impairment were investigated. Groups of guinea pigs were exposed to daily 3 1/2-hour presentations of 120 dB of broad-band noise in an atmosphere of either carbogen gas or normal air. Other groups received carbogen or normal air with a low intensity (50 dB) acoustic exposure. After a 30-day stabilization period each ear was examined electrophysiologically and histologically. Measures included a.c. cochlear potentials from 100 Hz through 20 kHz as well as counts of missing inner hair cells (IHCs) and outer hair cells (OHCs). Statistically significant improvement in the 1 microV isopotential function of the a.c. cochlear potential over all test frequencies and significant reduction in the number of missing IHCs and OHCs was found to result from inhalation of carbogen gas. Blood gas analysis demonstrated a rapid and marked elevation in arterial PCO2 and PO2 with a corresponding drop in pH to result from inhalation of carbogen. The vasodilating effects of increased arterial carbon dioxide tension are discussed in terms of current speculations regarding the role of vasoconstriction in noise-induced hearing loss.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood / Q000627:therapeutic use*; D003051:Cochlea / Q000473:pathology; D003055:Cochlear Microphonic Potentials; D006168:Guinea Pigs; D006198:Hair Cells, Auditory / Q000473:pathology; D006317:Hearing Loss, Noise-Induced / Q000209:etiology / Q000628:therapy*; D007759:Labyrinth Diseases / Q000628:therapy; D010100:Oxygen / Q000097:blood / Q000627:therapeutic use*; D012138:Respiratory Therapy
D002245:Carbon Dioxide; C011700:carbogen; D010100:Oxygen